Urinary protein loss (proteinuria) affects some 100 million people worldwide and is a feature of kidney dysfunction of glomerular origin and itself a risk factor for both renal and extra-renal diseases1. Kidney podocytes and their foot processes (FP) are a key component of the ultrafiltration system in the glomerulus where they comprise the filtration barrier together with endothelial cells and the glomerular basement membrane (GBM). Podocytes are located within the glomerulus of the kidney where they are attached to the GBM via α3β1 integrin2,3, and α/β dystroglycan4. Podocyte FPs are interconnected by the slit diaphragm (SD), a modified adherens junction5. Proteinuric kidney diseases are typically associated with various degrees of podocyte membrane remodeling (FP effacement and/or SD disruption) driven by a rearrangement of the podocyte microfilament system6. Recent work has advanced our understanding of the molecular framework underlying podocyte structure largely through the analysis of hereditary proteinuria syndromes and genetic models7. A few studies suggest also mechanisms for the far more common acquired proteinuric diseases8,9. Despite this progress, there are currently no cell-specific therapeutics for podocytes available. An emerging concept for the regulation of podocyte structure and function is the regulation of the podocyte cytoskeleton by proteases such as cathepsin L8,10. Cathepsin L induction in podocytes is accompanied by an increase in cell motility of cultured podocytes10. The increased motility of in vitro podocytes10, 11 is best translated into FP dynamics in vivo where podocytes remain locally attached to the GBM but may have altered FP dynamics resulting in FP fusion. In some forms of inflammatory glomerular diseases such as crescentic glomerulonephritis, podocytes have been reported to move out of their microenvironment into areas of crescentic glomerular damage12. The concept of dynamic podocyte FPs dates far back into the 1970's where elegant studies of Seiler and colleagues have shown that infusion of polycations such as protamine sulfate can induce rapid changes in FP dynamics and FP effacement13. Moreover, this event could be largely reversed by the infusion of polyanions such as heparin13. Even so it is impossible to image FP dynamics continuously in live animals, results from above studies suggest a highly dynamic podocyte FP system. Moreover the electron-microscopical analysis of normal kidney commonly reveals small areas of FP effacement which probably represents FPs during transition. Cancer cell motility is another example where cells can be hyperdynamic or participate in tissue invasion14.